Our studies further reveal the precise involvement of noradrenergic (NE) systems in the central regulation of LH release. In ovariectomized rats, the episodic secretion of LH is adversely altered by pharmacologic agents. Clonidine, alpha-adrenergic agonist, reinitiated pulsatile LH secretion in these drug treated rats, thereby suggesting the central NE neurons exert only a permissive influence on the pulsatile LH release. Furthermore, contrary to previous suggestions implicating NE as initiatior of LH pulses, we found that the pulsatile mechanism may predominantly be resident in the LHRH neurons. Studies utilizing the technique of destruction of NE by pharmacologic means have also identified the MPOA as a central locus where NE terminals communicate with LHRH containing neurons. These studies also showed that general anesthetics may drastically reduce hypothalamic NE activity in ovariectomized rats. This effect of anesthetics may be a mechanism whereby pentobarbital suppresses the secretory activity of the LHRH neurons. Another study also showed that NE neurons may mediate the effects of opiate agonists and antagonists, morphine and naloxone, respectively, on LH secretion and hence, modulation of LH release by endogenous opioid peptides may require NE participation.